Dysregulation of serum IgA underpins multiple pathologies. Selective IgA deficiency (sIgAD), the most common primary immunodeficiency, elevates risks for recurrent infections and autoimmune disorders like systemic lupus erythematosus (SLE) and celiac disease. Conversely, elevated serum IgA associates with IgA nephropathy, where galactose-deficient IgA1 deposits in renal glomeruli trigger complement-mediated inflammation and progressive kidney failure. Hyper-IgA levels may also signal immunodeficiency syndromes or multiple myeloma, particularly when beta-migrating monoclonal proteins complicate electrophoresis interpretation. The IgA2 subclass, distinguished by reduced sialylation, exhibits heightened pro-inflammatory activity linked to rheumatoid arthritis severity.

Clinically, serum IgA quantification aids immunodeficiency diagnosis and myeloma monitoring, where nephelometric assays outperform traditional electrophoresis. Therapeutic strategies targeting FcαRI or aberrant IgA production, such as monoclonal antibodies against B-cell activating factor (BAFF), show promise in autoimmune and renal diseases. Additionally, engineered IgA antibodies are being explored for enhanced neutrophil-mediated tumor cytotoxicity, highlighting its expanding translational potential.

Common uses include IVD Assay standards, calibrators and controls, therapeutics research, immune system research.